Making care primary: Medicare's latest attempt at value-based primary care.

On June 8th, 2023, the Centers for Medicare and Medicaid Innovation (CMMI) announced the Making Care Primary (MCP) model, its latest attempt to transform primary care delivery for a value-based care payment system. The MCP is a decade-long multi-payer partnership with a voluntary risk-adjusted payment model for primary care organizations. It provides financial support for organizations to develop and implement a value-based care infrastructure and prospective payments per beneficiary for the delivery of primary care. The MCP consists of 3 tracks, ranging from lump-sum infrastructure payments to a fully prospective payment model with 1-sided risk. In turn, physicians need to meet a set criteria, such as quality outcomes, health-related social needs screening and referral, and high-touch chronic care management (CMMI; https://innovation.cms.gov/innovation-models/making-care-primary). While MCP is a well-planned effort, it is likely to suffer from some of the same pitfalls as prior CMS attempts to revolutionize primary care and may therefore exert unintended effects on market consolidation.

Extracellular ATP-Induced Alterations in Extracellular H+ Fluxes From Cultured Cortical and Hippocampal Astrocytes.

Small alterations in the level of extracellular H+ can profoundly alter neuronal activity throughout the nervous system. In this study, self-referencing H+-selective microelectrodes were used to examine extracellular H+ fluxes from individual astrocytes. Activation of astrocytes cultured from mouse hippocampus and rat cortex with extracellular ATP produced a pronounced increase in extracellular H+ flux. The ATP-elicited increase in H+ flux appeared to be independent of bicarbonate transport, as ATP increased H+ flux regardless of whether the primary extracellular pH buffer was 26 mM bicarbonate or 1 mM HEPES, and persisted when atmospheric levels of CO2 were replaced by oxygen. Adenosine failed to elicit any change in extracellular H+ fluxes, and ATP-mediated increases in H+ flux were inhibited by the P2 inhibitors suramin and PPADS suggesting direct activation of ATP receptors. Extracellular ATP also induced an intracellular rise in calcium in cultured astrocytes, and ATP-induced rises in both calcium and H+ efflux were significantly attenuated when calcium re-loading into the endoplasmic reticulum was inhibited by thapsigargin. Replacement of extracellular sodium with choline did not significantly reduce the size of the ATP-induced increases in H+ flux, and the increases in H+ flux were not significantly affected by addition of EIPA, suggesting little involvement of Na+/H+ exchangers in ATP-elicited increases in H+ flux. Given the high sensitivity of voltage-sensitive calcium channels on neurons to small changes in levels of free H+, we hypothesize that the ATP-mediated extrusion of H+ from astrocytes may play a key role in regulating signaling at synapses within the nervous system.